Objective This study aimed to test the hypothesis that geniposide(GNP) protects against oxidative stress in early bRain injury(EBI)after experimental subarachnoid hemorrhage(SAH). Methods Male Wistar rats(n= 48) were randomly allocated to four groups, including the sham + vehicle group, SAH + vehicle group, SAH +GNP low dose group, and SAH + GNP high dose group. The experimental SAH model was established by injecting blood into the prechiasmatic cistern and treatments were then administered. Outcomes were measured at 24 hours after treatment. The SAH score and mortality rate were calculated. Nuclear factor erythroiD-2-related factor 2(Nrf2)expression in the temporal cortex was detected by immunofluorescence staining. Heme oxygenase-1(HO-1), NADPH quinineoxidoreductase-1(NQO-1), and glutathione S-transferase ( GST ) protein expression in the temporal cortex was determined by western blotting. Malondialdehyde(MDA)levels in the temporal cortex were detected by the thiobarbituric acid method . Apoptosis of nerve cells was determined using TUNEL staining. Results In the SAH+vehicle group, MDA levels and the rate of cellular apoptosis were significantly higher compared with those in the sham+vehicle group( both P<0. 05). The number of Nrf2- positive cells and HO-1, NQO-1, and GST expression were significantly higher in the SAH+vehicle group compared with the sham+vehicle group(all P<0. 05). Compared with the SAH+vehicle group, Ttreatment of either a high or low dose of GNP result ed in a higher number of Nrf2-positive cells and higher HO-1, NQO-1, and GST expression, and lower MDA levels and cellular apoptosis rate(all P<0. 05). In addition, Llower mortality was also observed in the SAH+GNP high dose group. group treated with a high dose of GNP(100 mg / kg). Conclusions GNP exerts a protective effect against oxidative stress in EBI after SAH. This effect is probably mediated by activating the Nrf2 pathway and upregulating the downstream of pathway—antioxidants.